The aim of this study is to provide understanding of the specific role of increased dispersion of ventricular refractoriness in the genesis of ventricular arrhythmias. In the animal model, we will test the effect of prolonged QT-interval associated with normal dispersion of refractoriness, and the effect of prolonged Qt-interval associated with nonhomogenous refractoriness within the left ventricle in the basic beats on the dispersion of refractoriness in the premature beats and the threshold for multiple responses induced by two successive ventricular premature stimuli. The magnitude of dispersion will be determined instantaneously from the differences between the points representing the ends of siz simultaneously recorded monophasic action potentials both in the basic and in the premature beats while the conduction within the studied region will be measured on the surface of the ventricle and across the wall. The objective of this study is to express the electrophysiologic characteristics of the studied region in precisely measured terms and identify the contribution of varying degree of accurately measured QT prolongation and dispersion of refractoriness to the genesis of ventricular arrhythmias which either occur spontaneously, or are induced by premature stimuli.